Doses from 1 to 10 sporulated oocysts of a cloned strain of Eimeria hungaryensis were used to infect laboratory-reared, coccidia-free wood mice (Apodemus sylvaticus). Total oocyst production, reproductive indices (output/dose) and daily patterns of oocyst production were compared. At doses of 10 oocysts or less, observed yields exceeded expected yields calculated using details of endogenous stages. At doses above 10 oocysts, the converse occurred. From infections initiated with 10 oocysts, total outputs were not significantly different in male and female wood mice, host age had no apparent effect and repeated infections, at 10-day intervals, of both sexes, resulted in progressive decreases in output at each successive infection, suggesting development of resistance.

An acoustic actograph was used to monitor for 17 days after infection the spontaneous flight activity of the mosquito Anopheles stephensi parasitized with the rodent malaria Plasmodium yoelii. Activity fell to approximately two-thirds of control levels at about day 10 post-infection – when oocysts were reaching maximum size and starting to rupture (mean number of oocysts = 92) – and thereafter remained at this reduced level. The circadian activity pattern was not affected by the parasitism.

Cystosporogenes operophterae, a microsporidian parasite of the winter moth, Operophera brumata, was cultured in a Spodoptera frugiperda cell line. The infected cultures were achieved by addition of haemolymph from larvae infected with C. operophterae. The infection rates for the cell line ranged from 80 to 95% after incubation for 10 days at 25 or 20 °C. There was no development in cultures incubated at 30 °C. Light and electron microscopy were used to observe the development of C. operophterae in vitro.

A steer was infected with Theileria parva parva Kilae stabilate; nymphal Rhipicephalus appendiculatus ticks were applied to its ears so that they completed repletion when the steer had a high piroplasm parasitaemia. The engorged nymphs were subsequently incubated at 28°C for 26–29 days to complete moulting, when the adult ticks were divided into two groups; one was incubated at 18°C for 20 days and the other at 18°C for 14 days and then at 37°C for 6 days. Groups of ticks incubated at 37 and 18°C were triturated and each resultant supernatant fluid inoculated into a steer. Both steers became infected, but the 37°C supernatant group showed a much shorter pre-patent period to schizonts. Groups of ticks incubated at 37 or 18°C were applied to pairs of cattle for 24, 48 and 72 h and then removed. There was a more rapid transmission of theileriosis to cattle by ticks kept at high ambient temperatures compared to those kept at low ambient temperatures. All cattle on which ticks treated at 37°C were applied developed acute and fatal T. parva infection irrespective of the duration of tick application, while only 1 animal receiving ticks treated at 18°C and fed for 72 h developed infection. The pre-patent period for macroschizonts was very short in all the groups receiving ticks incubated at 37°C. Mature sporozoites were detected in the salivary glands of unfed ticks incubated at 37°C and after they were applied to cattle for 24, 48 and 72 h but in those incubated at 18°C sporozoites were detected, only at 48 and 72 h after application.

Shared antigens between Brugia malayi and Aedes aegypti were studied. The experiments carried out with sera from infected Mastomys natalensis indicated that an immunological response against A. aegypti antigens (Mr 185, 35, 32 kDa) appeared often when animals became microfilaraemic and increased progressively in intensity during the time-course of infection. Sera of animals immunized with B. malayi reacted with the crude extract of mosquitoes and conversely, antibodies from animals immunized with A. aegypti reacted with the surface of B. malayi microfilariae. The implications of these findings for the natural history of B. malayi infection are discussed.

We have shown here that collagen type I bound efficiently to the trypomastigote surface. In addition, monoclonal and polyclonal antibodies against collagen types I and III inhibited the infection of fibroblasts by the parasite. These results suggested the presence of collagen-binding protein(s) on the parasite surface. This protein was identified from trypomastigote surface antigens using affinity chromatography on a Gelatin Ultrogel column (denatured form of collagen). These collagen-binding proteins were revealed as a low-affinity gelatin binding protein (LAG Bp) of 98 kDa, and a high-affinity binding protein (HAG Bp) of 58 and 68 kDa under non-reducing and reducing conditions respectively. In addition, HAG Bp and LAG Bp bound to collagen type I. The 58/68 kDa protein was purified to homogeneity on a wheat germ agglutinin Sepharose column. A polyclonal antibody to this glycoprotein, as well as a monoclonal antibody (McAb) 155D3 produced against the HAG Bp, immunoprecipitated two parasite surface antigens of 160 and 58 kDa under non-reducing conditions which migrated at a position of 80–85 and 68 kDa when reduced. However, only the 80–85 kDa component could be precipitated from [S] methionine-labelled trypomastigote antigens under reducing conditions. The antibodies to the 58/68 kDa glycoprotein as well as McAb 155D3 diminished the invasion of fibroblasts by parasites. Taken together these results suggest that the same receptor binds fibronectin and/or collagen and that both the 80–85 and 58/68 kDa glycoproteins form part of the same receptor. These trypomastigote surface molecules may interact with the host cell fibronectin and/or collagen during the initial phase of parasite-cell recognition.

A group of 27 variable antigen type (VAT)-specific monoclonal antibodies (McAbs) have been made against metacyclic forms of a cloned stock of Trypanosoma brucei rhodesiense. In combination, these labelled in immunofluorescence 99·3% of trypanosomes in salivary probes from tsetse flies. The 0·7% of unlabelled trypanosomes were believed to be uncoated forms. The ability of a mixture of antibodies to kill metacyclics in vitro by complement-mediated lysis, thus neutralizing their infectivity for mice, was tested. The antibody mixture consisted of 24 McAbs plus 3 VAT-specific rabbit antisera. In 12 replicate experiments this mixture of antibodies prevented infection of mice. Parallel controls showed that neutralization was probably antibody-mediated and VAT specific. However, we have not been able to repeat these results on a long-term basis; this may be due to a loss of neutralizing activity by one of the McAbs. The successful neutralization experiments indicate that the number of VATs in the metacyclic repertoire of one stock of T. b. rhodesiense is limited to at most 27.

In Trypanosome congolense, the surface antigens expressed by cultured metacyclic forms are a limited and serodeme-specific subset of variable antigen types (VATs). Experiments were carried out in mammalian-form (MF) cultures, comprising dividing trypanosomes which express metacyclic VATs (M-VATs) maintained in vitro with a mammalian cell feeder layer, or in mice following infection with cultured metacyclic populations. Selective neutralization experiments were performed by incubating populations of trypanosomes with one or a combination of McAbs to remove their respective M-VATs. Deletion of one M-VAT from the population had no effect on expression and growth of other unrelated M-VATs. Deleted M-VATs were detected in very small proportions of the total population 2–7 days following neutralization. Subsequent incubation of neutralized cultures resulted in growth of deleted M-VATs which, in most cases, reached pre-neutralization levels. It appears, therefore, that in conditions where expression of M-VATs on dividing trypanosomes occurs, removal of individual M-VATs results in their re-expression within the population.

Passive transfer experiments showed that 76% of the resistance induced in CBA/Ca mice by exposure to radiation-attenuated cercariae of Schistosoma mansoni could be transferred to naive recipients by administration of donor serum. The level of protection achieved depended on the volume of serum administered and immunity was demonstrated most consistently with serum harvested from thrice vaccinated donors. The serum was twice as effective when given to the recipients at the time of cercarial challenge as compared to administration 5 days after challenge, a result which indicates that serum-dependent challenge elimination is probably accomplished in the cutaneous tissues. This view was confirmed by the observation that passive protection could be ablated by administration of a monoclonal antibody which we have shown elsewhere to deplete the cutaneous inflammatory reaction to cercarial penetration. Histopathological studies revealed that vaccine serum induced subdermal inflammatory reactions in challenged recipient mice which were identical both in induration and kinetics to those seen in conventionally vaccinated individuals; on days 4 and 5 post-challenge, the reactions comprised 60% mononuclear cells and 40% eosinophils. Challenge larvae, which had transformed from skin-stage to lung-stage parasites, became trapped within such reactions and eventually showed generalized vacuolation consistent with the onset of damage. Some foci were seen to contain degenerated leucocytes, free eosinophil granules and debris which is thought to represent the remnants of dead parasites. Small focal reactions were identified on occasion in naive challenged mice and in recipients of normal mouse serum, but these reactions comprised predominantly mononuclear cells and were rarely seen to encompass challenge parasites. These data show that serum-transferred resistance in the vaccinated CBA/Ca mouse model involves the induction of a cutaneous inflammatory response in the recipients.

The techniques of generalized linear modelling were applied to worm burdens of 2268 mice artificially infected with Schistosoma mansoni and treated with oxamniquine and/or praziquantel. Models which maximized the Poisson likelihood were shown to be superior to those assuming either a log Normal or negative binomial error structure. Use of the models to calculate and compare ED values of 8 strains of S. mansoni, detect abnormal dose response and synergism and to pool data from several experiments is illustrated.

The cuticular permeability of anhydrobiotic 4th-stage juveniles of Ditylenchus dipsaci decreases during rehydration, as indicated by staining with osmium tetroxide, the measurement of permeability coefficients by the rate of uptake of tritiated water from a HOH/C-inulin bathing solution and by an increased ability to slow down the rate of water loss and to survive subsequent desiccation. The initial decrease in permeability coefficient is rapid, suggesting a physical effect due to the rehydration of the cuticle, followed by a slower reduction over the subsequent 1–4 h which is dependent upon metabolic activity. The reestablishment of the permeability barrier is sensitive to metabolic inhibitors which affect enzyme activity and post-transcriptional protein synthesis. Sodium iodoacetamide was the only inhibitor which affected maintenance of the permeability barrier. An Arrhenius plot of changes in cuticular permeability with temperature indicated a sharp increase in permeability at 40–50°C and brief exposure to diethyl ether resulted in loss of the permeability barrier, suggesting that a superficial layer, probably the epicuticle, is responsible for controlling cuticular permeability.

The role of the larva of the alder fly Sialis lutaria as a host for Neoechinorhynchus rutili (Acanthocephala) has been investigated. Brown trout (Salmo trutta) infected with N. rutili were found to be feeding on S. lutaria larvae which contained juvenile acanthocephalans in their haemocoels. These acanthocephalans have been identified as N. rutili. A previous report of this host-parasite relationship indicated some form of host response to the larval acanthocephalan. Stained wax sections of S. lutaria larvae infected with N. rutili did not show any evidence of either a host response or encapsulation. Samples of S. lutaria larvae revealed an interesting pattern of infection. Only larvae of a particular size range were infected. An experiment to infect commercially obtained rainbow trout (Salmo gairdneri) with N. rutili by feeding them with infected S. lutaria larvae was successful. Since S. lutaria larvae are known to be prey items for trout it appears that this route of infection could commonly occur in the natural environment. Larval S. lutaria is considered as an additional intermediate host to several ostracod species which have been shown to play a role in the transmission of N. rutili.

Field observations at one site on brown trout (Salmo trutta) and three-spined sticklebacks (Gasterosteus aculeatus) concurrently infected with mature Neoechinorhynchus rutili, together with the knowledge that large trout can be piscivorous in habit led to the proposition that the post-cyclic transmission of N. rutili may occur between these fish species. This route of transmission has been suggested for a number of acanthocephalan species. A laboratory experiement was conducted and it was demonstrated that uninfected rainbow trout (Salmo gairdneri) can acquire a N. rutili infection as a result of feeding on sticklebacks already carrying established worms in their intestines. This finding may help to explain how N. rutili is found in a wide range of fish definitive hosts throughout the northern holarctic region. More generally this example provides further evidence of the flexibility within acanthocephalan life-history patterns.

Three superoxide dismutases (SOD) (EC 1.15.1.1) were detected in homogenates of Ascaris suum. Each of the three forms of SOD was purified by a sequence of multiple differential centrifugations, ammonium sulphate precipitation, ion-exchange chromatography and G-75 Sephadex column chromatography. The three forms of SOD were present in different cellular locations; one in the cytoplasmic fraction, sensitive to cyanide and hydrogen peroxide, and two in the mitochondrial fraction, one of which was cyanide sensitive. The SOD forms presented clear differences in their electrophoretic patterns. The sexual organs of females showed the highest SOD activities of all the tissues examined. The finding of such high levels of superoxide dismutase in A. suum reflects the importance of this enzyme in the metabolism of this helminth parasite.

Parasitic helminths have an absolute requirement for carbohydrate for their energy metabolism, there being no significant contribution from fatty acid or amino acid catabolism. There is no significant synthesis of glucose or glycogen from non-hexose precursors in helminths and so they are dependent on dietary carbohydrate. Characteristically parasitic helminths break down glycogen or glucose via linear anaerobic pathways to give reduced organic end-products, usually acids such as lactate, acetate, succinate and propionate or more rarely alcohols such as ethanol, propanol and acetoin (Barrett, 1984).